widely available, vastly reducing the lethal menace of bacteria, we can guess confidently that the Next Big One will be a virus too.
To understand why some outbreaks of viral disease go big, others go really big, and still others sputter intermittently or pass away without causing devastation, consider two aspects of a virus in action: transmissibility and virulence. These are crucial parameters, defining and fateful, like speed and mass. Along with a few other factors, they largely determine the gross impact of any outbreak. Neither of the two is an absolute constant; they vary, they’re relative. They reflect the connectedness of a virus to its host and its wider world. They measure situations, not just microbes. Transmissibility and virulence: the yin and yang of viral ecology.
You’ve heard a bit already about transmissibility, including the simple statement that viral survival demands replication and transmission. Replication can occur only within cells of a host, for the reasons I’ve mentioned. Transmission is travel from one host to another, and transmissibility is the packet of attributes for achieving it. Can the virions concentrate themselves in a host’s throat or nasal passages, cause irritation there, and come blasting out on the force of a cough or a sneeze? Once launched into the environment, can they resist desiccation and ultraviolet light for at least a few minutes? Can they invade a new individual by settling onto other mucous membranes—in the nostrils, in the throat, in the eyes—and gaining attachment, cell entry, another round of replication? If so, that virus is highly transmissible. It goes airborne from one host to another.
Fortunately, not every virus can do that. If HIV-1 could, you and I might already be dead. If the rabies virus could, it would be the most horrific pathogen on the planet. The influenzas are well adapted for airborne transmission, which is why a new strain can circle the world within days. The SARS virus travels this route too, or anyway by the respiratory droplets of sneezes and coughs—hanging in the air of a hotel corridor, moving through the cabin of an airplane—and that capacity, combined with its case fatality rate of almost 10 percent, is what made it so scary in 2003 to the people who understood it best. But other viruses employ other means of transmission, each with its own advantages and limitations.
The oral-fecal route sounds disgusting but is really quite common. It works well for some viruses because host creatures (including humans) are often forced, especially when living at high densities, to consume food or water contaminated by excrement from other members of their population. This is one of the reasons why children die of dehydration in rainy refugee camps. The virus goes in the mouth, replicates in the belly or the intestines, causes gastrointestinal distress, may or may not spread to other parts of the body, and comes gushing out the anus. Diarrhea, for such a virus, is part of an effective strategy for dispersal. Viruses transmitted this way tend to be fairly hardy in the environment, because they may need to linger in that polluted sump for a day or two before some desperate person comes to drink from it. There’s an entire group of such viruses, known as the enteroviruses, including polio and about seventy others, that attack us in the gut. Most of those enteroviruses are uniquely human infections, not zoonoses. Evidently they don’t need other animal hosts for maintaining themselves in a crowded human world.
For blood-borne viruses, transmission is more complicated. Generally it depends on a third party, a vector. The virus must replicate abundantly in the blood of the host to produce severe viremia (that is, a flood of virions). The vector (a blood-sucking insect or some other arthropod) must arrive for a meal, bite the host, slurp up virions along with the blood, and carry them away. The vector itself must be a hospitable host, so that the virus replicates further within it, producing many more virions that make their way back to the mouth area and stand ready for release. Then the vector must drool virions (as anticoagulant saliva) into the next host it bites. The yellow fever virus, West Nile, and dengue transmit this way. It has an upside and a down.
The downside is that vector transmission requires adaptations for two very different sorts of environment: the bloodstream of a vertebrate and the belly of an arthropod. What works well in one may not work at all in the other, so the virus must carry